Low sodium diet and adipokine secretion: Implications for the cardiovascular system?

Abstract

The influence of dietary sodium intake on cardiovascular risk factors has been a matter of decade-long discussions. Needed is a clear-cut elucidation of the beneficial mechanisms of action of reduced salt intake. In a recent study, lean and obese mice were subjected to a high or low salt diet for 16 weeks. The low salt diet tremendously reduced fasting insulin in obese animals, and HOMA-IR was improved. Reduced adiponectin expression in the heart and in peritoneal adipose tissue in obese animals was restored or even increased compared to normal levels with the low salt diet. Corresponding with the beneficial effect on adiponectin, inflammatory markers were reduced to lean levels by the low salt diet. Whether the increase in adiponectin would have been larger if the rise in aldosterone had been prevented is one of the questions raised by this study. The data obtained in this animal study are based on a robust methodological basis for two reasons: first, the long-term intervention of 16 weeks clearly represents a strength of the study; second, dietary sodium restriction was modest, as judged by only 2-fold increased plasma renin activity. Overall, the data presented by Baudrand et al. in the current issue of NMCD may path the way to a better understanding of the mode of action of modest sodium restriction. However, a replication of the results in a more human-like diet-induced obesity mouse model is warranted.